Psychological factors such as hypnosis, emotion, stress, and attention produce powerful modulatory effects on nociception and pain. However, the influence of attention on nociception and pain and the underlying neural mechanism responsible are unclear. The current literature on attentional modulation of spinal nociceptive responses, as measured by the RIII reflex, and pain perception (pain intensity) is inconsistent and often contradictory. The present thesis provides a new component-based framework for the examination of attentional modulation of the RIII reflex and pain. A delayed-discrimination task was decomposed into the three components of attention – namely alerting, orienting, and executive control (sensory working memory). Previously, the multidimensional nature of attention was largely ignored in the pain literature. We show that each component of attention exerts a distinct modulatory effect on nociception and pain and suggest that this accounts for some of the confusion in the literature. By considering stress separately, we demonstrate for the first time that stress blocks attentional modulation of the RIII reflex, indicating an interaction and dissociation of attention- and stress-mediated modulation of spinal nociceptive responses. This important finding clarifies much of the disagreement in the literature, since cognitive tasks often induce increases in stress that consequently confound interpretation. Additionally, both visual and somatosensory stimuli were included in the discrimination task, revealing that the influence of attention on pain intensity is spatially-specific whereas attentional modulation of nociception is modality-specific, at least for the modalities investigated. From these findings a component-based model for the attentional modulation of pain processes is proposed. This model is substantially supported by the literature and provides a meaningful and cohesive explanation of the seemingly contradictory results across studies. Moreover, this model suggests potential neural mechanisms underlying the attentional modulation of pain.